[Imaging findings of carcinoma ex pleomorphic adenoma in minor salivary glands].

PURPOSE: To summarize the CT and MR imaging features of carcinoma ex pleomorphic adenoma(Ca-ex-PA) in minor salivary gland, and analyze the correlation between various features and pathological classification. METHODS: Forty-three patients with Ca-ex-PA in minor salivary gland were collected. The CT and MRI findings were retrospectively analyzed and correlated with their pathological types. Fisher's exact test was used to analyze the correlation between various imaging features (tumor morphology, boundary, internal structure, bone invasion, cervical lymph node metastasis) and pathological types with SPSS 25.0 software package. RESULTS: Among the 43 patients with Ca-ex-PA, 83.7%(36/43) of the tumors were lobulated; 81.4%(35/43) showed cystic degeneration or necrosis, with heterogeneous enhancement. Coarse calcification or mixed calcification was found in 37.2%(16/43), 25.6%(11/43) had compressive absorption of adjacent bone. 75%(12/16) of type Ⅰ/Ⅱ tumors had regular morphology (round or oval), and 77.8%(21/27) of type Ⅲ tumors had irregular morphology, 93.8%(15/16) of type Ⅰ/Ⅱ tumors had well-defined margin and 66.7%(18/27) of type Ⅲ tumors had ill-defined margin. Osteolytic bone resorption occurred in 59.3%(16/27) of type Ⅲ tumors. The average maximum diameter of type Ⅰ/Ⅱ tumors was significantly shorter than that of type Ⅲ(P＜0.05). Fisher's exact test showed the characteristics of tumor morphology, boundary and osteolytic bone resorption were related to pathological grouping(P＜0.001). CONCLUSIONS: Most Ca-ex-PA in minor salivary glands is characterized by lobular and heterogeneous enhanced neoplasm on CT and MR imaging. A round or oval tumor with well-defined margin usually correlates with typeⅠ and Ⅱ, contrarily, an irregular mass with ill-defined margin and osteolytic bone destruction usually correlates with type Ⅲ. Combining the three characteristics of morphology, boundary and osteolysis is more helpful to distinguish type Ⅰ/Ⅱ and type Ⅲ tumors.

Cardiomyocyte mitochondrial dynamic-related lncRNA 1 (CMDL-1) may serve as a potential therapeutic target in doxorubicin cardiotoxicity.

Doxorubicin (DOX)-induced cardiotoxicity has been one of the major limitations for its clinical use. Although extensive studies have been conducted to decipher the molecular mechanisms underlying DOX cardiotoxicity, no effective preventive or therapeutic measures have yet been identified. Microarray analysis showed that multiple long non-coding RNAs (lncRNAs) are differentially expressed between control- and DOX-treated cardiomyocytes. Functional enrichment analysis indicated that the differentially expressed genes are annotated to cardiac hypertrophic pathways. Among differentially expressed lncRNAs, cardiomyocyte mitochondrial dynamic-related lncRNA 1 (CMDL-1) is the most significantly downregulated lncRNA in cardiomyocytes after DOX exposure. The protein-RNA interaction analysis showed that CMDL-1 may target dynamin-related protein 1 (Drp1). Mechanistic analysis shows that lentiviral overexpression of CMDL-1 prevents DOX-induced mitochondrial fission and apoptosis in cardiomyocytes. However, overexpression of CMDL-1 cannot effectively reduce mitochondrial fission when Drp1 is minimally expressed by small interfering RNA Drp1 (siDrp1). Overexpression of CMDL-1 promotes the association between CMDL-1 and Drp1, as well as with phosphorylated (p-)Drp1, as evidenced by RNA immunoprecipitation analysis. These data indicate the role of CMDL-1 in posttranslational modification of a target protein via regulating its phosphorylation. Collectively, our data indicate that CMDL-1 may play an anti-apoptotic role in DOX cardiotoxicity by regulating Drp1 S637 phosphorylation. Thus, CMDL-1 may serve as a potential therapeutic target in DOX cardiotoxicity.

KDM4B promotes gastric cancer metastasis by regulating miR-125b-mediated activation of Wnt signaling.

Emerging evidence has demonstrated that the aberrant expression of histone-modifying enzymes such as histone demethylases contributes to gastric carcinogenesis and progression. The role of KDM4B in cancer progression has been gradually revealed. However, the underlying mechanisms regulating gastric cancer metastasis of KDM4B remain unclear. In the present study we determined KDM4B expression in gastric cancer and its biologic function in vitro and in vivo. We found that KDM4B expression was significantly increased in most gastric cancer tissues compared with the adjacent normal tissues. Upregulated expression of KDM4B in human gastric cancer was correlated with poor prognosis. In vitro, KDM4B overexpression in AGS cells promoted cell invasion, whereas knockdown of KDM4B inhibited cell invasion. Furthermore, KDM4B overexpression also promoted tumor metastasis in vivo. Mechanistically, KDM4B upregulated miR-125b expression and activated Wnt signaling pathway. More important, miR-125b partially mediated KDM4B-induced activation of Wnt signaling. Finally, we demonstrated that KDM4B promoted gastric cancer cell invasion in vitro and cancer metastasis in vivo, at least in part, by upregulating miR-125b expression. These data provided novel insights on the role of KDM4B-driven gastric cancer metastasis and indicated that KDM4B may be served as a potential target for gastric cancer.

P2Y6 contributes to ovalbumin-induced allergic asthma by enhancing mast cell function in mice.

Extracelluar nucleotides have been identified as regulatory factors in asthmatic pathogenesis by activating purinergic receptors. This research aimed to investigate the function of the purinergic receptor P2Y6 in mediating airway inflammation in allergic asthma. Wild-type (WT) and P2Y6-deficient mice were stimulated with ovalbumin (OVA) to construct asthmatic mouse models. Overexpression of P2Y6 and uridine 5'-diphosphate (UDP)-releasing were demonstrated in lung tissues in ovalbumin-induced asthmatic mice. The release of the cytokine IL-4, mast cell invasion, and the airway remodeling phenotypes were more severe following the application of UDP in asthmatic mice. However, P2Y6 deficiency reduced these asthmatic pathogeneticsymptoms markedly in a mouse model. In vitro, we found that P2Y6 in purified mast cells enhanced the functions of mast cells in the inflammatory response in the asthmatic process by triggering their capability for migration, cytokine secretion and granule release. Moreover, P2Y6 stimulated the function of mast cells through activation of the AKT signaling pathway. Our data provides evidence that P2Y6 contributes to allergic airway inflammation and remodeling by enhancing the functions of mast cells in ovalbumin-induced asthmatic mice.

Analysis of whole genomic expression profiles of Helicobacter pylori related chronic atrophic gastritis with IL-1B-31CC/-511TT genotypes.

OBJECTIVE: Many studies have linked cytokine interleukin-1B gene polymorphisms to H. pylori-related gastric cancer development. The current study evaluated the characterization of whole genomic expression profiles of the premalignant condition: H. pylori-related chronic atrophic gastritis (CAG) with IL-1B-31CC/-511TT genotypes. METHODS: IL-1B-31/-511 gene polymorphisms were determined by DNA sequences. RNA was extracted and expression profiles were performed using Agilent human whole genomic oligonucleotide microarrays (G4112F). The expression of three samples with H. pylori infection was compared to that of three samples without H. pylori infection from samples of six CAG patients, all with IL-1B-31CC/-511TT genotypes. Differentially expressed genes related to H. pylori-induced CAG with IL-1B-31CC/-511TT genotypes were screened and analyzed further by Gene Ontology (GO) and pathway. Validation of the microarray data was performed using qRT-PCR. RESULTS: A total of 124 differentially expressed genes and 32 GO term annotations were identified between H. pylori positive and negative groups in the six CAG samples with IL-1B-31CC/-511TT genotypes. The signaling pathways identified were oxidative phosphorylation and epithelial cell signaling in H. pylori infection. Five overlapping genes were contained in identified GO terms and pathways: ATP6V0B, NDUFS5, NDUFV2, ATP6V1F and ATP6V1G1. Comparisons of qRT-PCR data and the previously reported data with the results of gene chips support the validity of our microarray data. CONCLUSION: The H. pylori-related CAG with IL-1B-31CC/-511TT genotypes has shown to be the more malignant phenotype than H. pylori negative CAG with IL-1B-31CC/-511TT genotypes. Mitochondrial energy metabolism probably plays a crucial role as it is the molecular mechanism of host-bacterial interactions.

[Imaging features and differentiated diagnosis of desmoplastic fibroma of the jaw bones].

PURPOSE: To investigate the imaging feature of desmoplastic fibroma (DF) of the jaw bones. METHODS: The records including diagnostic radiograph images of 8 patients were retrospectively analyzed. The age of the 8 patients ranged from 2 years to 70 years (means,28 years). The numbers of males and females were 3 and 5 respectively. Of 8 patients, 4 had local recurrence, which occurred 1 year after curettage. RESULTS: On conventional radiographs, the lesion was presented as a purely lytic tumor that did not contain any mineralized matrix. The zone of transition between tumor and normal bone was typically narrow and well defined but not sclerotic. Bone expansion in DF had an eccentric (n=3) and lace-like, reticular pattern (n=3). On CT scan, increased bone marrow density (n=3), a homogeneous soft-tissue density mass displaced adjacent muscle with lingual cortex eroded (n=3) were noted. On MRI, the lesion was displayed as large bony destruction area, with homogeneous hypointensity on T1-weighted images, non-homogenous hyperintensity on T2-weighted and did not enhance after Gd-DTPA administration. Images with Choline peek (Cho, at 3.2 ppm) was displayed at TE of 144 ms( PRESS, single voxel).Six mandibular cases and 2 maxillary tumors were located posteriorly. CONCLUSIONS: Recognition of DF is important because DF is more aggressive than other benign fibrous lesions, necessitating a wide surgical and careful long-term follow-up for local recurrence.

[Imaging diagnosis of myoepithelioma of the salivary glands].

PURPOSE: To investigate CT imaging and clinical features of myoepithelioma (ME) of the salivary glands. METHODS: The imaging manifestations of 17 patients from 2003 to 2007 were retrospectively analyzed. The age of the 17 patients ranged from 23 years to 70 years (mean age: 46 years). The numbers of males and females were 7 and 10, respectively. RESULTS: The diameter of the lesions were less than 2.5 cm. 13 of the lesions located in the major salivary glands, were shallow, mostly contacted with the capsule of the gland (12/13) with obvious nodular enhancement. 4 of the lesions were located in the minor salivary glands with non-enhancement. The palate plate was absorbed with compression (2/3). CONCLUSIONS: Understanding of the imaging and clinical characteristics of ME can increase the accuracy of diagnosis.

[Decreased peripheral nerve conduction velocity may be associated with lower-serum level of vitamin E in patients with infantile hepatitis syndrome].

OBJECTIVE: To explore the influence of vitamin E (VitE) concentration in serum on peripheral nerve conduction in patients with infantile hepatitis syndrome (IHS). METHODS: A retrospective study was carried out in 58 infants suffered from IHS without congenital biliary atresia and 31 of them were followed up. Thirty-two healthy infants were as control. The level of VitE in serum was detected with high performance liquid chromatography and nerve conduction was tested with surface electrodes along the nerves of limbs. The relationship between the level of VitE or total bilirubin (TB) or direct bilirubin (DB) and the nerve conduction velocity was analyzed comparatively. RESULTS: (1) The serum level of VitE was below the lower limit of 90% the normal value (13.78 micromol/L) in 71% (41/58) of patients, and was below the lower limit of 99% the normal level (9.17 micromol/L) in 48% (28/58) of patients. (2) The level of DB was more than 25.7 micromol/L in 86% (50/58) of the patients and was more than 102.6 micromol/L in 47% (27/58) of patients. Severe conjugated hyperbilirubinemia with cholestasis was demonstrated in most patients. (3) At least one abnormal parameter in nerve conduction test was found in 86% (50/58) patients. In 144 nerves tested, 60.4% (87/144) had at least one abnormal parameter. (4) Analysis for the association between bilirubin levels and VitE concentration in serum: in groups of DB > or = 25.7 micromol/L and DB < 25.7 micromol/L, the percentage of decreased VitE concentrations was 78% (39/50) and 25% (2/8), respectively, and the difference was significant (P < 0.01). Similar association between low VitE concentration and increased level of TB in serum could not be demonstrated. (5) Analysis for the association between abnormal nerve conduction and VitE concentration in serum: in the two groups with low and normal level of VitE, the percentage of abnormal nerve conduction was 93% (38/41) and 71% (12/17), respectively (chi(c)(2) = 4.93, P < 0.05). (6) Analysis for the association between abnormal nerve conduction and bilirubin in serum: There was no significant association between abnormal nerve conduction and serum level of either DB or TB. (7) Eight patients died and 9 patients had motor development delay in 31 patients during follow up. In these 17 patients with poor outcome, 88% (15/17) had very low VitE levels (< 9.17 micromol/L), which was markedly higher than the proportion of cases (43%, 6/14) with better prognosis (chi(c)(2) = 7.235, P < 0.01). CONCLUSIONS: (1) Low VitE serum levels were found in excess of the two thirds of patients with IHS and severely decreased levels in nearly a half of them. (2) A conjugated hyperbilirubinemia with cholestasis could be found in most patients (86%) suffered from IHS without congenital biliary atresia and about a half of them had serious cholestasis. (3) Conjugated hyperbilirubinemia with cholestasis could be the predominant cause of decreased serum VitE level in this study. (4) Abnormality of nerve conduction in patients with IHS might be related to VitE deficiency.